Comparative analysis of the sequence and structure of two Drosophila melanogaster genes encoding vitelline membrane proteins

A 36-kb genomic DNA segment of the Drosophila melanogaster genome containing 12 clustered cuticle genes has been mapped and partially sequenced. The cluster maps at 65A 5-6 on the left arm of the third chromosome, in agreement with the previously determined location of a putative cluster encompassing the genes for the third instar larval cuticle proteins LCP5, LCP6 and LCP8. This cluster is the largest cuticle gene cluster discovered to date and shows a number of surprising features that explain in part the genetic complexity of the LCP5, LCP6 and LCP8 loci. The genes encoding LCP5 and LCP8 are multiple copy genes and the presence of extensive similarity in their coding regions gives the first evidence for gene conversion in cuticle genes. In addition, five genes in the cluster are intronless. Four of these five have arisen by retroposition. The other genes in the cluster have a single intron located at an unusual location for insect cuticle genes.

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Phenotypic interactions of spinster with the genes encoding proteins for cell death control in Drosophila melanogaster

Archives of Insect Biochemistry and Physiology ◽

10.1002/arch.20345 ◽

2010 ◽

Vol 73 (3) ◽

pp. 119-127 ◽

Cited By ~ 5

Author(s):

Akira Sakurai ◽

Yoshiro Nakano ◽

Masayuki Koganezawa ◽

Daisuke Yamamoto

Keyword(s):

Cell Death ◽

Drosophila Melanogaster ◽

Genes Encoding

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A Family of Genes Clustered at the Triplo-lethal Locus of Drosophila melanogaster Has an Unusual Evolutionary History and Significant Synteny With Anopheles gambiae

Genetics ◽

10.1093/genetics/165.2.613 ◽

2003 ◽

Vol 165 (2) ◽

pp. 613-621 ◽

Cited By ~ 2

Author(s):

Douglas R Dorer ◽

Jamie A Rudnick ◽

Etsuko N Moriyama ◽

Alan C Christensen

Keyword(s):

Phylogenetic Analysis ◽

Drosophila Melanogaster ◽

Anopheles Gambiae ◽

Evolutionary History ◽

Codon Bias ◽

Good Target ◽

The Family ◽

Genes Encoding ◽

And Function ◽

Gambiae Genome

Abstract Within the unique Triplo-lethal region (Tpl) of the Drosophila melanogaster genome we have found a cluster of 20 genes encoding a novel family of proteins. This family is also present in the Anopheles gambiae genome and displays remarkable synteny and sequence conservation with the Drosophila cluster. The family is also present in the sequenced genome of D. pseudoobscura, and homologs have been found in Aedes aegypti mosquitoes and in four other insect orders, but it is not present in the sequenced genome of any noninsect species. Phylogenetic analysis suggests that the cluster evolved prior to the divergence of Drosophila and Anopheles (250 MYA) and has been highly conserved since. The ratio of synonymous to nonsynonymous substitutions and the high codon bias suggest that there has been selection on this family both for expression level and function. We hypothesize that this gene family is Tpl, name it the Osiris family, and consider possible functions. We also predict that this family of proteins, due to the unique dosage sensitivity and the lack of homologs in noninsect species, would be a good target for genetic engineering or novel insecticides.

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Craniofacial Diseases Caused by Defects in Intracellular Trafficking

Genes ◽

10.3390/genes12050726 ◽

2021 ◽

Vol 12 (5) ◽

pp. 726

Author(s):

Chung-Ling Lu ◽

Jinoh Kim

Keyword(s):

Endoplasmic Reticulum ◽

Membrane Proteins ◽

Intracellular Trafficking ◽

Critical Role ◽

Treatment Strategies ◽

Soluble Proteins ◽

Genes Encoding ◽

Membrane Bound ◽

Signaling Receptors ◽

Craniofacial Morphogenesis

Cells use membrane-bound carriers to transport cargo molecules like membrane proteins and soluble proteins, to their destinations. Many signaling receptors and ligands are synthesized in the endoplasmic reticulum and are transported to their destinations through intracellular trafficking pathways. Some of the signaling molecules play a critical role in craniofacial morphogenesis. Not surprisingly, variants in the genes encoding intracellular trafficking machinery can cause craniofacial diseases. Despite the fundamental importance of the trafficking pathways in craniofacial morphogenesis, relatively less emphasis is placed on this topic, thus far. Here, we describe craniofacial diseases caused by lesions in the intracellular trafficking machinery and possible treatment strategies for such diseases.

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Differential elimination of rDNA genes in bobbed mutants of Drosophila melanogaster

Molecular and Cellular Biology ◽

10.1128/mcb.6.4.1023-1031.1986 ◽

1986 ◽

Vol 6 (4) ◽

pp. 1023-1031

Author(s):

R Terracol ◽

N Prud'homme

Keyword(s):

Drosophila Melanogaster ◽

Gene Copy Number ◽

Rdna Locus ◽

Gene Copy ◽

Specific Gene ◽

Type I ◽

28S Rrna ◽

Wild Type ◽

Y Chromosomes ◽

Genes Encoding

In Drosophila melanogaster, the multiply repeated genes encoding 18S and 28S rRNA are located on the X and Y chromosomes. A large percentage of these repeats are interrupted in the 28S region by insertions of two types. We compared the restriction patterns from a subcloned wild-type Oregon R strain to those of spontaneous and ethyl methanesulfonate-induced bobbed mutants. Bobbed mutations were found to be deficiencies that modified the organization of the rDNA locus. Genes without insertions were deleted about twice as often as genes with type I insertions. Type II insertion genes were not decreased in number, except in the mutant having the most bobbed phenotype. Reversion to wild type was associated with an increase in gene copy number, affecting exclusively genes without insertions. One hypothesis which explains these results is the partial clustering of genes by type. The initial deletion could then be due either to an unequal crossover or to loss of material without exchange. Some of our findings indicated that deletion may be associated with an amplification phenomenon, the magnitude of which would be dependent on the amount of clustering of specific gene types at the locus.

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